Andrew Vaughan, Ph.D.

Specialties

Department

Title

Clinical Interests

One of the earliest steps in either the generation of leukemia, or the genesis of a solid tumor is a break in DNA that is mis-repaired. In each case, the null hypothesis is that such breaks occur at random. In the case of leukemia, it is apparent that such breaks may be targeted to specific genes by aberrant action of normal gene products such as Activation Induced Cytidine Deaminase (AID). For the generation of solid tumors, the deletion of large tracts of DNA containing tumor suppressor genes may also be regulated by local DNA secondary structure and/or epigenetic modification. Proof of cellular control over such early events in tumorigenesis would disprove the null hypothesis and open up new areas for suppressing such tumor promoting events.